[Mysteries of viral latency and reactivation]

Varicella-zoster virus is a Herpesvirus responsible for three distinct clinical features: chicken pox (varicella), shingles (herpes zoster) and post-zosterian pain (post-herpetic neuralgia). Neurological features of these diseases such as complications of chicken pox, viral latency in sensory ganglia and reactivation as shingles with concurrent and possibly subsequent prolonged pain, are the sequels of the invasion of the peripheral nervous system during primary infection. Prevention is achieved by vaccination with a live attenuated virus strain and therapy calls for specific antiviral agents. In many respects, vzv behaves differently from close relatives. In particular, viral latency in the nervous system is basically different from that of other Herpesviridae. The recent discovery of the expression of some viral regulatory proteins during latency, although it had always been considered that vzv latency was silent, and demonstration that these proteins are immunogenic open new avenues concerning the immune control of vzv reactivation.